Surgery chapters

Pancreas: complications of acute pancreatitis, pseudocyst and pancreatic cancer

The surgical side of the pancreas: causes, severity scoring and management of acute pancreatitis, its local and systemic complications including necrosis and pseudocyst, chronic pancreatitis in brief, and carcinoma of the pancreas and ampulla.

UHS PGET syllabus: Abdomen and abdominal wall (16 MCQs, both groups), PancreasUpdated October 2026
In 30 seconds
  • Acute pancreatitis is diagnosed by typical pain plus amylase or lipase above 3 times normal (or CT); commonest causes are gallstones and alcohol; severity is judged by persistent organ failure (revised Atlanta) and scores such as Glasgow-Imrie or Ranson (3 or more = severe) and CRP above 150 mg/L at 48 hours.
  • Treatment is supportive (fluids, analgesia, early enteral feeding); urgent ERCP only for gallstone pancreatitis with cholangitis or persisting obstruction; cholecystectomy in the same admission for mild gallstone attacks. Infected necrosis (gas on CT) is treated by step-up: antibiotics, percutaneous or endoscopic drainage, then minimally invasive necrosectomy.
  • A pseudocyst is an amylase-rich collection with a fibrous wall (no epithelium) at 4 weeks or more; most resolve, while persistent, large or symptomatic ones are drained (endoscopic or surgical cystgastrostomy). Pancreatic cancer (ductal adenocarcinoma, mostly in the head) gives painless progressive jaundice with a palpable gallbladder; few are resectable (Whipple or PPPD).
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Overview

The pancreas lies retroperitoneally across the posterior abdominal wall. Its head sits in the C-loop of the duodenum, with the superior mesenteric vessels behind the neck, and the tail reaches the splenic hilum. Surgeons manage pancreatitis and its complications (necrosis, collections, pseudocysts, bleeding) and pancreatic and periampullary cancers.

Acute pancreatitis

Definition: acute inflammation of the pancreas from premature activation of enzymes (trypsin) inside the gland, causing autodigestion, inflammation, and in severe cases necrosis and a systemic inflammatory response.

Causes ("I GET SMASHED")

CauseNotes
Gallstones (commonest, about half)Small stones passing through the ampulla; women, older patients
Ethanol (alcohol)Second commonest; men
TraumaBlunt epigastric injury (handlebar, steering wheel)
Steroids and other drugsAzathioprine, thiazides, valproate, oestrogens
Mumps and other virusesCoxsackie, CMV
AutoimmuneIgG4-related disease
Scorpion venom
Hypercalcaemia, Hypertriglyceridaemia (very high), hypothermia
ERCPPost-ERCP pancreatitis occurs in a small percentage of procedures
IdiopathicSearch for microlithiasis and tumours

Clinical features

  • Sudden, severe, constant epigastric pain radiating to the back, eased by leaning forward; repeated vomiting.
  • Tachycardia, fever, epigastric tenderness, guarding; distension and ileus.
  • Mild jaundice in gallstone pancreatitis; swinging fever suggests cholangitis.
  • Bruising from retroperitoneal bleeding in severe cases: Grey Turner sign (flanks) and Cullen sign (periumbilical). Neither is specific (Cullen sign was first described with ruptured ectopic pregnancy).
  • Hypocalcaemia (fat saponification) can cause tetany.

Investigations

  • Serum amylase above 3 times the upper limit supports the diagnosis; lipase is more sensitive and specific and stays raised longer. A normal amylase does not exclude pancreatitis (late presentation, alcoholic or hypertriglyceridaemic attacks).
  • Other causes of raised amylase: perforated peptic ulcer, mesenteric ischaemia, intestinal obstruction, ruptured ectopic pregnancy, ruptured aortic aneurysm, renal failure, salivary gland disease, macroamylasaemia.
  • Ultrasound in every patient: to look for gallstones and a dilated CBD.
  • Erect chest X-ray: excludes perforation; may show pleural effusion (often left) or ARDS. Abdominal X-ray may show a sentinel loop or colon cut-off sign.
  • Contrast-enhanced CT: if the diagnosis is uncertain, or after about 72 hours in a severe or non-improving attack to show necrosis (non-enhancing pancreas) and collections. Early CT underestimates necrosis.
  • Bloods for scoring: FBC, U&E, glucose, calcium, albumin, LFTs, LDH, arterial gases, CRP.

Severity assessment

Glasgow (modified Imrie), within 48 hoursRanson, on admissionRanson, within 48 hours
PaO2 below 8 kPa (60 mmHg)Age above 55Haematocrit fall 10% or more
Age above 55White cells above 16 × 10^9/LUrea (BUN) rise despite fluids
Neutrophils (white cells) above 15 × 10^9/LGlucose above 11.1 mmol/LCalcium below 2.0 mmol/L
Calcium below 2.0 mmol/LLDH above 350 U/LPaO2 below 8 kPa
Renal: urea above 16 mmol/LAST above 250 U/LBase deficit above 4 mmol/L
Enzymes: LDH above 600 U/LFluid sequestration above 6 L
Albumin below 32 g/L
Sugar: glucose above 10 mmol/L

Three or more positive criteria (Glasgow or Ranson) predicts a severe attack. Other markers: CRP above 150 mg/L at 48 hours, APACHE II, BMI over 30, persistent SIRS.

Worked example: Glasgow-Imrie score

A 62-year-old: white cells 17 × 10^9/L, glucose 12 mmol/L, urea 9 mmol/L, calcium 2.2 mmol/L, albumin 30 g/L, LDH 450 U/L, PaO2 9.5 kPa
Positive: age above 55 (1), white cells above 15 (1), glucose above 10 (1), albumin below 32 (1)
Total = 4 → predicted severe attack (3 or more)

Revised Atlanta classification (2012):

GradeDefinition
MildNeither organ failure nor any local or systemic complication
Moderately severeTransient organ failure (settles within 48 hours) and/or local or systemic complications
SeverePersistent organ failure (beyond 48 hours), one or more systems
High-yield

The single best marker of a severe attack is organ failure that persists beyond 48 hours.

Management

  1. Supportive care in a monitored setting (HDU or ICU if severe): oxygen, goal-directed IV fluids (crystalloid), urinary catheter, analgesia (opioids are acceptable), glucose and electrolyte control.
  2. Nutrition: feed early by mouth or enteral tube; nasogastric feeding is acceptable, nasojejunal if not tolerated. Enteral feeding protects the gut barrier and lowers infection; there is no benefit in "resting" the pancreas. Parenteral nutrition only if enteral feeding fails.
  3. Antibiotics: not routinely given as prophylaxis; use them for cholangitis or proven or strongly suspected infected necrosis (carbapenems penetrate necrotic tissue well).
  4. Urgent ERCP (within about 72 hours) with sphincterotomy for gallstone pancreatitis with cholangitis or ongoing biliary obstruction (rising bilirubin, dilated CBD). It is not indicated for mild gallstone pancreatitis without obstruction.
  5. Cholecystectomy for gallstone pancreatitis: same admission for mild attacks (to prevent recurrence); after the collections settle in severe attacks. Sphincterotomy alone if unfit.
  6. Treat the cause: alcohol cessation, lower triglycerides, correct calcium, stop drugs.
Exam trap

Older teaching said "no enteral feeding in severe pancreatitis". Current practice is the opposite: early enteral feeding is preferred to parenteral nutrition.

Complications

SystemicLocal
SIRS, shock, ARDS, pleural effusionAcute peripancreatic fluid collection (early, no wall, mostly resolves)
Acute kidney injuryAcute necrotic collection (early necrosis, no wall) → walled-off necrosis (after about 4 weeks)
DIC, hyperglycaemia, hypocalcaemiaInfected necrosis, pancreatic abscess
Multiorgan failurePseudocyst
Pseudoaneurysm and haemorrhage (splenic, gastroduodenal artery); splenic or portal vein thrombosis (gastric varices)
Pancreatic ascites and pleural effusion (duct disruption); duodenal or colonic necrosis, fistulae; abdominal compartment syndrome

Deaths occur in two peaks: early (first week) from multiorgan failure, and late (after 2 weeks) from infected necrosis and sepsis.

Pancreatic necrosis

  • Non-enhancing pancreatic tissue on contrast CT.
  • Sterile necrosis: managed conservatively; do not drain or operate.
  • Infected necrosis: suspect when a patient with necrosis develops new fever, sepsis or worsening organ failure, usually after the second week; gas bubbles in the collection on CT are diagnostic; CT- or EUS-guided aspiration for culture if unsure. Mortality can reach about 50%.
  • Step-up approach for infected necrosis:

1. Antibiotics (for example a carbapenem). 2. Percutaneous (retroperitoneal) drainage or endoscopic transgastric drainage, ideally once the collection has walled off (about 4 weeks). 3. Minimally invasive necrosectomy (video-assisted retroperitoneal debridement or endoscopic necrosectomy). 4. Open necrosectomy with lavage is the last resort.

  • Early open surgery (in the first 2 weeks) has a high mortality and should be avoided.

Pancreatic pseudocyst

Definition: a collection of amylase-rich fluid contained within a mature wall made of fibrous or granulation tissue, with no epithelial lining, usually outside the pancreas, formed 4 weeks or more after an attack of acute pancreatitis (or with chronic pancreatitis or trauma). Most lie in the lesser sac behind the stomach. Many communicate with the main pancreatic duct.

Clinical features: persistent pain, early satiety, nausea and vomiting (gastric compression), an epigastric mass, persistently raised amylase, weight loss; jaundice if it compresses the CBD.

Investigations:

  • Ultrasound (follow-up) and CT (best for size, wall and relation to the stomach).
  • EUS with fluid aspiration to exclude a cystic neoplasm: pseudocyst fluid has high amylase and low CEA; a high CEA (above about 400 ng/mL) suggests a mucinous neoplasm.
  • MRCP or ERCP shows duct communication and strictures.

Complications: infection (abscess), haemorrhage (pseudoaneurysm of a nearby artery bleeding into the cyst), rupture into the gut or peritoneum (pancreatic ascites), gastric outlet or biliary obstruction, splenic vein thrombosis.

Management:

  • Most resolve spontaneously: observe with serial ultrasound if small and symptomless.
  • Less likely to resolve: larger than 6 cm, present more than 12 weeks, thick wall, chronic pancreatitis, duct stricture.
  • Drain if symptomatic, enlarging or complicated, once the wall has matured (about 6 weeks):
MethodNotes
Endoscopic cystgastrostomy or cystduodenostomy (EUS-guided, stents)First choice for a cyst bulging into the stomach or duodenum
Surgical internal drainageCystgastrostomy (cyst behind the stomach), Roux-en-Y cystojejunostomy (cyst not adherent to the stomach), cystduodenostomy (head of pancreas); laparoscopic or open; biopsy the wall to exclude neoplasm
Percutaneous external drainageFor infected cysts or unfit patients; risk of a persistent external pancreatic fistula
Transpapillary drainage (ERCP stent)Small cysts communicating with the duct
Excision (distal pancreatectomy)Selected tail pseudocysts
  • Bleeding pseudoaneurysm: angiographic embolisation first.
Exam trap

Do not drain an immature pseudocyst internally (the wall will not hold sutures), and do not mistake a cystic neoplasm for a pseudocyst: a cyst without a history of pancreatitis needs EUS and fluid analysis.

Chronic pancreatitis (brief)

  • Irreversible fibrosis with loss of exocrine and endocrine function; alcohol is the main cause; also hereditary, autoimmune, obstructive, tropical (calcific) pancreatitis in South Asia.
  • Chronic epigastric pain radiating to the back, steatorrhoea, diabetes, weight loss; calcification on X-ray or CT; dilated "chain of lakes" duct on MRCP.
  • Treatment: stop alcohol and smoking, analgesia, pancreatic enzyme replacement, insulin; endoscopic stenting or stone removal; surgery for intractable pain: lateral pancreaticojejunostomy (Puestow) for a dilated duct, Frey or Beger procedures for an enlarged head; resection if cancer cannot be excluded.

Carcinoma of the pancreas

Risk factors

  • Smoking (most important modifiable risk), age (peak 65-75), male sex.
  • Chronic pancreatitis, hereditary pancreatitis, long-standing or new-onset diabetes, obesity.
  • Family history and syndromes: BRCA2, Lynch syndrome, Peutz-Jeghers, familial atypical multiple mole melanoma; FAP for ampullary and duodenal cancer.

Pathology

  • More than 85% are ductal adenocarcinoma; most arise in the head.
  • Desmoplastic stroma; spreads early along nerves (perineural), lymphatics and veins; liver and peritoneal metastases are common.
  • Periampullary tumours (ampulla, distal CBD, duodenum, head of pancreas) present in the same way; ampullary tumours present early and have a much better prognosis.
  • Cystic neoplasms: serous cystadenoma (benign, honeycomb), mucinous cystic neoplasm (women, body or tail, ovarian-type stroma) and IPMN (intraductal papillary mucinous neoplasm; mucin extruding from a "fish mouth" ampulla); mucinous lesions are premalignant.
  • Neuroendocrine tumours: insulinoma (commonest; Whipple triad), gastrinoma (Zollinger-Ellison, in the gastrinoma triangle).

Clinical features

SitePresentation
Head and periampullaryPainless, progressive obstructive jaundice, pruritus, dark urine, pale stools, palpable gallbladder (Courvoisier), weight loss; ampullary tumours may give fluctuating jaundice and melaena (bleeding tumour; "silver stools")
Body and tailLate presentation with weight loss and back pain (coeliac plexus invasion, usually unresectable); no jaundice until spread
GeneralNew-onset diabetes over 50 without obesity or family history, unexplained pancreatitis, migratory thrombophlebitis (Trousseau sign), depression, gastric outlet obstruction, Virchow node, ascites, liver metastases

Investigations

  1. Ultrasound: dilated bile ducts (double duct sign with a dilated pancreatic duct).
  2. Pancreatic protocol contrast CT (the key test): shows the tumour, resectability and metastases.
  3. EUS with fine needle aspiration for small tumours and tissue diagnosis (needed before chemotherapy; not always required before resection of a clearly resectable mass).
  4. ERCP for brushing cytology and biliary stenting (for cholangitis, severe jaundice or delayed surgery); MRCP.
  5. CA 19-9: neither specific nor sensitive; useful as a baseline and for follow-up (also raised in obstructive jaundice).
  6. Staging laparoscopy for small liver and peritoneal deposits; PET-CT in selected cases.

Resectability

  • Unresectable: distant metastases (liver, peritoneum, distant nodes) or encasement of the superior mesenteric artery, coeliac axis or common hepatic artery.
  • Not a contraindication: tumour size alone, invasion of duodenum, and limited abutment of the portal or superior mesenteric vein (the vein can be resected and reconstructed).
  • At presentation, more than 85% are not resectable.

Surgery

  • Head, ampulla or distal CBD: pylorus-preserving pancreatoduodenectomy (PPPD) or the classic Whipple operation (also removes the gastric antrum). Removes the pancreatic head, duodenum, distal CBD and gallbladder; reconstruction with pancreaticojejunostomy (or pancreaticogastrostomy), hepaticojejunostomy and duodenojejunostomy (or gastrojejunostomy).
  • Body and tail: distal pancreatectomy with splenectomy.
  • Complications: postoperative pancreatic fistula (leak from the pancreatic anastomosis; the main cause of morbidity), delayed gastric emptying, post-pancreatectomy haemorrhage (often from a pseudoaneurysm after a leak), bile leak, intra-abdominal abscess, diabetes and exocrine insufficiency.
  • Adjuvant chemotherapy for about 6 months (gemcitabine-based, capecitabine combinations or modified FOLFIRINOX) improves survival; neoadjuvant treatment for borderline resectable tumours.

Palliation

ProblemTreatment
JaundiceEndoscopic (ERCP) self-expanding metal stent; PTC stent if ERCP fails; surgical hepaticojejunostomy (or choledochojejunostomy) at laparotomy
Gastric outlet obstructionEndoscopic duodenal stent or gastrojejunostomy
PainOpioids; coeliac plexus block (EUS or percutaneous)
Steatorrhoea, weight lossPancreatic enzyme replacement, nutrition
Disease controlPalliative chemotherapy (FOLFIRINOX or gemcitabine-based)

Overall prognosis is poor; even after resection most patients relapse, while ampullary cancers do considerably better.

Memory hook

Courvoisier in the head, back pain in the tail.

Exam focus

Expect: commonest causes (gallstones, alcohol); amylase and lipase cut-off and other causes of raised amylase (perforated ulcer); Glasgow and Ranson criteria (serum potassium is not a criterion), CRP above 150 mg/L and revised Atlanta severity grades; Grey Turner and Cullen signs; indications for urgent ERCP; early enteral feeding and no routine prophylactic antibiotics; timing of cholecystectomy; sterile vs infected necrosis (gas on CT) and the step-up approach; pseudocyst definition (no epithelial lining, 4 weeks), complications and cystgastrostomy; splenic vein thrombosis; risk factors for pancreatic cancer (smoking), painless jaundice with palpable gallbladder, double duct sign, CA 19-9, resectability (SMA encasement) and Whipple or PPPD; palliation with stents.

Quick revision

  • Causes: gallstones (commonest), alcohol, then the rest of I GET SMASHED.
  • Diagnosis: pain plus amylase or lipase more than 3 times normal; ultrasound for stones; CT after 72 hours for necrosis.
  • Severe: Glasgow or Ranson 3 or more, CRP above 150 at 48 h, persistent organ failure beyond 48 h.
  • Treatment: fluids, analgesia, early enteral feeding; ERCP only for cholangitis or obstruction; cholecystectomy in the same admission if mild.
  • Infected necrosis: gas on CT; antibiotics then step-up drainage and minimally invasive necrosectomy.
  • Pseudocyst: fibrous wall, no epithelium, 4 weeks; drain if symptomatic, large or persistent; endoscopic or surgical cystgastrostomy.
  • Pancreatic cancer: smoking; head; painless jaundice, palpable gallbladder; CT; CA 19-9; Whipple or PPPD if resectable; stents for palliation.

Written by The House Job from standard references (Bailey & Love).

FAQ

Is a normal amylase enough to rule out acute pancreatitis?

No. Amylase may be normal in late presentations and in alcoholic or hypertriglyceridaemic attacks; lipase or CT is used when doubt remains.

Should all patients with severe pancreatitis get prophylactic antibiotics?

No. Antibiotics are kept for cholangitis, other proven infections and suspected or confirmed infected necrosis.

How is a pseudocyst different from a true cyst?

A pseudocyst has a wall of fibrous or granulation tissue with no epithelial lining, while true cysts and cystic neoplasms are lined by epithelium.

When is ERCP needed in gallstone pancreatitis?

When there is cholangitis or continuing biliary obstruction, such as a rising bilirubin or a dilated common bile duct with a retained stone.

What makes a pancreatic head cancer unresectable?

Distant metastases or encasement of the superior mesenteric artery, coeliac axis or hepatic artery; limited involvement of the portal or superior mesenteric vein can still be resected.